Cardiovascular diseases and disorders are a major contributor to patient illness and mortality. They are also a primary driver of health care expenditure, costing billions of dollars each year in the United States. Common cardiovascular diseases and disorders include hypertension, ischemic heart disease, heart failure, and others. Hypertension, or high blood pressure, is a major cardiovascular disorder that is estimated to affect 65 million people in the United States alone. Of those with hypertension, it is reported that fewer than 30% have their blood pressure under control. Hypertension is a leading cause of heart failure and stroke. It is the primary cause of death for tens of thousands of patients per year and is listed as a primary or contributing cause of death for hundreds of thousands of patients per year in the U.S. Accordingly, hypertension is a serious health problem demanding significant research and development for the treatment thereof.
Hypertension occurs when the body's smaller blood vessels (arterioles) constrict, causing an increase in blood pressure. Because the blood vessels constrict, the heart must work harder to maintain blood flow at the higher pressures. Although the body may tolerate short periods of increased blood pressure, sustained hypertension may eventually result in damage to multiple body organs, including the kidneys, brain, eyes and other tissues, causing a variety of maladies associated therewith. The elevated blood pressure may also damage the lining of the blood vessels, accelerating the process of atherosclerosis and increasing the likelihood that a blood clot may develop. This could lead to a heart attack and/or stroke. Sustained high blood pressure may eventually result in an enlarged and damaged heart (hypertrophy), which may lead to heart failure.
Heart failure is the final common expression of a variety of cardiovascular disorders, including ischemic heart disease. Heart failure is characterized by an inability of the heart to pump enough blood to meet the body's needs and results in fatigue, reduced exercise capacity and poor survival. Heart failure results in the activation of a number of body systems to compensate for the heart's inability to pump sufficient blood. Many of these responses are mediated by an increase in the level of activation of the sympathetic nervous system, as well as by activation of multiple other neurohormonal responses. Generally speaking, this sympathetic nervous system activation signals the heart to increase heart rate and force of contraction to increase the cardiac output; it signals the kidneys to expand the blood volume by retaining sodium and water; and it signals the arterioles to constrict to elevate the blood pressure. The cardiac, renal and vascular responses increase the workload of the heart, further accelerating myocardial damage and exacerbating the heart failure state. Accordingly, it is desirable to reduce the level of sympathetic nervous system activation in order to stop or at least minimize this vicious cycle and thereby treat or manage the heart failure.
A number of drug treatments have been proposed for the management of hypertension, heart failure and other cardiovascular disorders. These include vasodilators to reduce the blood pressure and ease the workload of the heart, diuretics to reduce fluid overload, inhibitors and blocking agents of the body's neurohormonal responses, and other medicaments.
Various surgical procedures have also been proposed for these maladies. For example, heart transplantation has been proposed for patients who suffer from severe, refractory heart failure. Alternatively, an implantable medical device such as a ventricular assist device (VAD) may be implanted in the chest to increase the pumping action of the heart. Alternatively, an intra-aortic balloon pump (IABP) may be used for maintaining heart function for short periods of time, but typically no longer than one month. Cardiac resynchronization therapy (CRT) may be used to improve the coordination of the heart's contractions. Other surgical procedures are available as well.
It is known that the wall of the carotid sinus, a structure at the bifurcation of the common carotid arteries, contains stretch receptors (baroreceptors) that are sensitive to the blood pressure. These receptors send signals via the carotid sinus nerve to the brain, which in turn regulates the cardiovascular system to maintain normal blood pressure (the baroreflex), in part through activation of the sympathetic nervous system. Electrical stimulation of the carotid sinus nerve (baropacing) has previously been proposed to reduce blood pressure and the workload of the heart in the treatment of high blood pressure and angina. For example, U.S. Pat. No. 6,073,048 to Kieval et al. discloses a baroreflex modulation system and method for stimulating the baroreflex arc based on various cardiovascular and pulmonary parameters. Implantable devices for treating high blood pressure or hypertension by stimulating various nerves and tissue in the body are known and described, for example, in U.S. Pat. No. 3,650,277 (stimulation of carotid sinus nerve), U.S. Pat. No. 5,707,400 (stimulation of vagal nerve), and U.S. Pat. No. 6,522,926 (stimulation of baroreceptors).
Regardless of the treatment given to a patient, it is often desirable to monitor various physiological parameters of the patient, especially in conjunction with a delivered therapy. With implantable devices, physiological measurement and diagnostic data gathering may be done independently of therapy stimulation. For example, in a cardiac rhythm management device a dedicated sense amplifier channel is often implemented separately from the stimulation output channel, so that physiological measurements of heart rate, P-wave amplitude, R-wave amplitude, and QRS interval are done independently of device stimulation. The stimulation output is also independent of the monitoring of physiologic parameters such as minute ventilation, for which impedance measurements are taken across a pair of electrodes typically positioned at a distance suitable for a transthoracic measurement and not directly used for stimulation. The dedicated sense electrodes are excited with a signal source not used in the actual therapy. The signal sources for this kind of sensing are typically very low in amplitude and can cover a large stimulation vector.
Other current methods of measuring patient physiologic parameters such as blood pressure include direct intravascular or external blood pressure cuff determinations. Direct intravascular measurement is accomplished using complicated, discrete sensors separately located within the body, which require additional circuitry to be implanted into the body and may create difficulties for measuring the parameters in real time. Blood pressure measurement by an external cuff such as a sphygmomanometer allows for only sporadic monitoring.
The above methods each have their own disadvantages. Accordingly, it would be desirable for improved devices and methods to monitor patient physiologic parameters, either as a stand-alone device or combined with a delivered therapy.